A young male with unknown past medical history presents with AMS and tachycardia. EMS was called by a roommate after the patient was noticed to be nonverbal and lethargic. He reportedly took meth and had a recent drinking binge, but has not had alcohol for the last 2 days. His HR was 160 on arrival of EMS, and they gave him adenosine 6 mg and 12 mg and 500 cc NS, but with no response. The preshospital ECG and strips are not available. The patient was restless, agitated, and nonverbal on arrival to ED, with elevated HR at 150. Here is the first ED ECG:

What is the likely diagnosis?

There is sinus tachycardia, a prolonged QRS (computer read it as 114 ms, previous ECG with 102 ms). There is a large R-wave in lead aVR. These findings are nearly pathognomonic of, or at least highly suspicious for, tricyclic antidepressant (TCA) overdose.

In addition, the QT interval is 360, and the Bazett-corrected QT interval (QTc) is 540 ms.

One can read about management of TCA overdose in many places, and I have put some links to lifeinthefastlane below.

A few important points:

1. An R-wave in lead aVR greater than 3 mm, or an R/S ratio greater than 0.7, is highly suspicious for sodium channel blockade, which is the most important of the many toxicities of TCA overdose.

2.In 49 patients with known TCA overdose, a maximum limb lead QRS duration greater than 100 ms was 100% sensitive for detecting patients who will seize, and seizure is a harbinger of cardiovascular collapse. At this cutoff of 100 ms, however, the specificity was not perfect. Of 11 patients with an initial QRS duration of 100-119 ms, 2 (18%) had seizures, and of 22 with an initial QRS duration of 100-139 ms, 4 (18%) had seizures. Of 14 with initial QRS of 140 ms or longer, 8 (56%) had seizures. No patient with a QRS of less than 160 ms had ventricular dysrhythmias.

2a. In an unselected population with suspicion of overdose, a minimally wide QRS (less than 110 ms) will be much less specific; furthermore, it is likely that frequent serial ECGs, by detecting an increasing QRS duration, will detect those at risk of toxicity. On the other hand, administration of bicarbonate, the antidote, is relatively safe compared with a seizure. If the diagnosis is unclear, narrowing of a widened QRS on ECG following sodium bicarbonate administration (1-2meq/kg) adds further support that pharmacologic sodium blockade is present.

When it became clear that the patient had sinus tach and not PSVT, his presentation was recognized as an overdose or drug toxicitiy. But because the physicians were so focused on his tachycardia, meth use, and rhythm, they did not look for or appreciate the findings of TCA overdose. We in emergency medicine obtain ECGs in overdoses mostly to look for TCA findings. So when you get an ECG in this situation, look for them!

Much later, the roommate called and reported that 20 amitryptiline (unknown mg per dose) were missing. Fortunately, the patient had not had any adverse outcome by that time.
He was given multiple amps of bicarb and a bicarbonate drip. He remained delirious and was given 3 mg of physostigmine (after pretreatment with 2 mg of lorazepam to prophylax against seizures). His delirium greatly improved and he was then able to follow commands.

He had a prolonged stay in the ICU requiring days of bicarbonate. The tox screen only showed amitryptiline.

Tuesday, March 29, 2016

An otherwise healthy woman in her 20's with no past medical history presented with tachycardia. She had experienced palpitations and called 911. Prehospital rhythm strips were at a rate of at least 200 (unavailable) and the medics gave adenosine at both 6 mg and 12 mg with no effect. She was stable, with no CP, SOB, hypotension or evidence of shock.

Here is the initial ED ECG:

What is the diagnosis (this is pathognomonic)? See below. (Notice that the computer incorrectly read ***Acute MI***)

1. The rhythm is irregularly irregular, therefore it is atrial fibrillation
2. The complexes are wide (so one might think of atrial fibrillation with aberrancy, in which case you should see RBBB or LBBB pattern, which is not there)
3. It is very fast (200 bpm)
4. The shortest R-R interval (between complexes 12 and 13) is about 240 ms (very short)
5. The complexes look bizarre and multiform. They are not uniform, as they would be with simple aberrancy. Thus, these represent differentially pre-excited ventricular myocardium.

This is atrial fibrillation in the setting of WPW, and is a dangerous rhythm which can degenerate into ventricular fibrillation. It is more likely to degenerate if the physicians gives AV nodal blocking drugs, including adenosine (so the medics were lucky they did not make things worse), but especially calcium channel blockers.

How should this be managed? It can be managed with medications that convert atrial fibrillation to sinus, such as procainamide or ibutilide (and others), but when you have a wide complex very fast tachycardia, it is best to use electrical cardioversion. It is the safest, and keeps you from having to make a definite diagnosis.As long as you can manage procedural sedation, which is very easy in the case of cardioversion because you only need seconds of sedation and amnesia, then cardioversion is the safest method.

Even in the ED, the pattern was not recognized as atrial fibrillation with pre-excitation, but as atrial fib with aberrancy. These were very smart and very experienced physicians, but anyone can make a snap judgment followed by premature closure (this is another reason why electricity is the safest - you don't need to have the correct diagnosis).

Subsequently, the physicians gave the patient first diltiazem and then esmolol, with no ill effect but also little beneficial effect. They were lucky they did not make things worse. Either of these medications, but especially the diltiazem, could have resulted in Ventricular Fibrillation. AV nodal blockade is particularly dangerous when there is a shortest R-R interval of less than 250 ms (as here), and especially if less than 220 ms. As I mentioned above, adenosine is also contraindicated.

After dialing up the esmolol, the patient spontaneously converted to NSR and had the following ECG:

Sinus rhythm with short PR interval and large delta waves seen best in precordial leads, and confirming Wolff Parkinson White (WPW) syndrome of pre-excitation down an accessory pathway. There can be positive, negative, or isoelectric delta waves depending on their own axis. WPW may greatly change both depolarization (in this case with large upright R-waves in right precordial leads because the accessory pathway is left lateral, depolarizing the ventricle from left to right) and repolarization (see these cases for acute MI mimics due to WPW)

Followup, and what is "Concealed Conduction"?

Her charts revealed 3 previous visits for palpitations, and in all cases the ECG was interpreted as normal. Here is one of them:

There are very subtle delta waves which were not noticed by the computer algorithm or by the reading physician. The computer read a QRS duration of 106 ms which is borderline long and due to these subtle delta waves. The PR interval is normal because the delta waves are so minimal.

When the delta wave is absent, it is sometimes called concealed conduction. In this case, it is nearly concealed. That is to say, the presence of an accessory pathway is not obvious (at least to most observers) on the baseline surface ECG. (There are times when it is truly concealed, and there are no delta waves even in retrospect). It is important to know about concealed conduction so that if you suspect WPW as a cause of tachycardia that is now resolved, you will not rule out the diagnosis by a normal baseline ECG.

There are two mechanisms of concealed conduction:

1. Conduction through the accessory pathway is retrograde only (mechanism unclear)
2. The impulse reaches the AV node and gets through to the ventricles before it gets to, and through, the accessory pathway.

The second mechanism applies in this case: Look at the first two ECGs above (those with abnormal conduction). Notice that the R-wave in V1 is very large, as it would be in RBBB. This is because the impulse is going down a left lateral bypass tract and then proceeding through the myocardium from left to right, resulting in a large R-wave in V1. Thus, the bypass tract (accessory pathway) is to the left lateral of the left atrium, which is far from the sinus node (right part of right atrium). When the AV node is conducting fast (such as with anxiety, low vagal tone, high catecholamines, etc.), then the impulse gets to and through the AV node and through the Purkinje system before it makes it down the accessory pathway and therefore there is no (or minimal) delta wave. On the other hand, if the AV node conduction is slower, then the delta waves will be evident.

However, even in WPW with concealed conduction, the accessory pathway is always available to cause trouble!

In both types of concealed conduction, it can result in orthodromic reciprocating supraventricular tachycardia (re-entrant down through the AV node and up through the bypass tract), and this cannot be differentiated from intranodal reentrant (standard) SVT on the surface ECG.

Saturday, March 26, 2016

This was contributed by Rohin Francis (Twitter: @MedCrisis), a cardiologist from England and FOAM enthusiast.

Case

A 55 year old lady initially presented to hospital with an acutely ischaemic arm. An embolic occlusion of her brachial artery was diagnosed by CT and treated with anticoagulation. The following day she developed sudden severe chest pain. This ECG was obtained:

Sinus rhythm.The rather alarming appearance of the QRST may be mistaken for a broad complex QRS but, in fact, her QRS complex can be clearly seen in V2, V3 and II and is
narrow. What has manifested as triangular complexes is actually huge ST
segment elevation seen in V2-5 and laterally in I and aVL. There is also
ST segment depression inferiorly. A proximal LAD occlusion can produce
anterolateral ST elevation, but if the circumflex is also occluded, it
is possible the anterior ST elevation might be attenuated and indeed
here the ST elevation is less pronounced in V2 and V3.

Smith comment:Note there is ST depression in aVR, a true sign of Left Main occlusion. Many authors state that ST elevation in aVR is a good ECG sign of left main occlusion. This is erroneous. (See this post for more explanation).ST elevation in aVR is a sign of left main or 3 vessel insufficiency (not occlusion), due to diffuse subendocardial ischemia, which results in leftward and anterior ST depression (towards lead II and V5) and reciprocal ST elevation in aVR.Left main occlusion is identical to simultaneous occlusion of the Proximal LAD (anterolateral STE: STE in V2-V6, I, aVL) and circumflex (posterolateral STE: STE in aVL, STD in V1-V4). The opposing ST vectors of anterior and posterior can (at least partly) cancel each other out in V1-V4, so that the lateral has the most obvious STE, as in this case. Lead aVR is opposite an imaginary lead between leads I and II, often called (-aVR). You can see that left main occlusion causes high lateral STE (aVL) with reciprocal STD (leads II and III); since aVR is reciprocal to this ST elevation, there is ST depression in lead aVR.

Case continued

She was immediately transferred to the primary PCI centre. On
arrival she was in cardiogenic shock and haemodynamically unstable. Her
BP was 80 systolic, GCS 13 and she had a grey appearance.

An
intra-aortic balloon pump was inserted first and the cardiac arrest and
ECMO teams were alerted. This was the initial shot of her angiogram:

The guide catheter was deliberately not engaged with the left main artery, as an occlusion was suspected. Here one can see contrast being injected
towards the left main and a large thrombus sitting at the ostium. A
small amount of flow is passing but not reaching further than proximal
circumflex nor LAD. There is sluggish clearance of contrast from the aortic
root indicative of poor cardiac output. An intra-aortic balloon pump
can be seen inflating and deflating in the descending aorta.Smith comment: There is near total obstruction of the Left Main. I am no angiographer, but I believe that this is TIMI-1 flow, which results in ST elevation. It is not TIMI-0 flow (total obstruction/occlusion), as some minimal contrast gets through. All thrombi are dynamic, however, and the only certainty one can have about the condition of the artery 45 minutes earlier, during recording of the ECG, comes from ECG analysis.

Passing angioplasty wires into her coronary arteries restored flow to
the circumflex but not LAD. Her left main and LAD were opened using very
careful aspiration and she received a drug eluting stent to her
proximal left main.

Here is the aspirated thrombus:

Large red thrombus aspirated

Despite revascularisation and inotropic support, she remained in
cardiogenic shock. An on-table echocardiogram revealed severe global
impairment of her left ventricle. She was shocked out of VF on several
occasions but continued to arrest so was placed onto femoral VA ECMO.

Peripheral
ECMO increases afterload by introducing blood into the aorta and if
there is no cardiac ejection, it can cause dilatation of the LV.
Unfortunately despite maximal therapy in ICU, she continued to
deteriorate.

A trans-oesophageal
echocardiogram revealed extensive thrombus in the aortic root and left
ventricle. She died later that day. A post mortem was not performed but
disparate embolic events in her arm and coronary circulation might point
to an intra-cardiac source of thrombus. Thrombi tend to form in
impaired ventricles, but it is unclear if the severe left failure seen
on echo was pre-existing or simply a result of a catastrophic acute
coronary syndrome.

Thursday, March 24, 2016

We just published this case report, the full text of which you can read here. The ECG is diagnostic of coronary occlusion also, but many interventionalists might not believe the ECG. Speckle tracking proves it.

It is tempting to think that the waves before the QRS are large P-waves, but in fact one can discern P-waves within these large waves (see V2 in particular).

Thus, these are very late T-waves. Thus the QT interval is very long. I measure the QT interval at about 520 ms. Since the RR interval is about 560 ms, then the Bazett-corrected QTc is about 690 ms (very long). What part of the QT interval is long? Is the T-wave itself very wide? Is the time from T-wave peak to T-wave end (T-peak to T-end, or TpTe, long)? No! TpTe is perhaps the best predictor of Torsade de Pointe (TdP).The long QT is due to a very long ST segment. This is pathognomonic of hypocalcemia. The fact that hypocalcemia affects the ST segment and not the TpTe interval may account for the fact that TdP from long QT due to hypocalcemia is exceedingly rare, with only a few case reports (in which the etiologic link to low calcium is not even definitely established). In hypocalcemia (long ST, but NOT a wide T-wave, not a long TpTe), depolarization has a long duration, but repolarization occurs relatively quickly. The ionized calcium was 1.08 mg/dL. I do not have information on the etiology.

Clinical history

This was an elderly woman who presented with altered mental status. Vital signs were normal except for an oxygen saturation of 91% and temperature of 35C.

Exam had peripheral vasoconstriction, but otherwise normal

Bedside US: normal

Chest x-ray: normal

No tetany!

Calcium gluconate was given.

After the Ca was replenished to 4.09 mg/dL, this ECG was recorded:

The T-waves are somewhat flat, but you can see that the QT interval is now about 370 ms, QTc about 460 ms, and a normal ST segment.

The patient's mental status normalized.
The etiology of the hypocalcemia was not investigated.

Learning Points:

1. Hypocalcemia causes a long QT by lengthening the ST segment.
2. The T-wave duration, specifically the TpTe does not lengthen
3. It is a long TpTe which is most responsible for Torsades in long QT
4. Thus, long QT in hypocalcemia does not appear to have nearly the risk of long QT from other etiologies.

T-Peak to T-end (TpTe)

This comes from a manuscript that Dr. Ken Dodd and I have written. Ken was my primary co-author on the derivation of the Modified Sgarbossa Criteria.

"In patients with normal conduction, the TpTe interval has
been noted to prolong during myocardial ischemia and correct after reperfusion [1, 2]. It has also been claimed to predict
mortality after myocardial infarction and has been called the best determinant
of TdP development in the setting of acquired bradydysrhythmias [3]. In patients with LBBB, prolongation
of the TpTe has been shown to be independently associated with sudden cardiac
death [4]."

Monday, March 21, 2016

This late middle-aged male had sudden onset of chest pressure. Here is the prehospital ECG:

The rhythm is a bit hard to discern. It appears to be sinus with PACs.It is obviously an anterior (and lateral) STEMI. What other ominous finding is present?

The cath lab was activated prehospital, and on arrival, the patient was in shock, with hypotension and an StO2 of 55% (this is a tissue oxygen saturation; normal is 75%. 55% represents shock no matter what the blood pressure). He denied SOB but immediate bedside ultrasound showed B-lines of pulmonary edema. Oxygen saturations were 94% on nasal cannula. BP was approximately 90 systolic.

Here is the ED ECG:

Now there is atrial fibrillation with moderately rapid ventricular rate (126)There is huge ST elevation in V2-V4 and I and aVL, diagnostic of proximal LAD occlusionHere is the ominous finding: Right Bundle Branch Block (RBBB) + LAFB (left anterior fascicular block).

A proximal LAD thrombotic occlusion was opened. Here is the post-reperfusion ECG:

Sinus rhythm at a rate of 117. Uncertain if conversion was spontaneous, or done electrically in the cath labRBBB and LAFB persist (not a good sign).ST elevation is greatly improved (a good sign), though still very elevated (not a good sign).There is terminal T-wave inversion, an early sign of reperfusion.

A balloon pump was placed.

Here is the ECG the next day:

Q-waves and poor R-wave progression. RBBB and LAFB are gone. (A good sign).

Highest troponin I was extremely high at 230 ng/mL at 10 hours after arrival.

Echo showed anterolateral wall motion abnormality and EF of 35%.

In spite of maximal supportive therapy, balloon pump, and persistently open arteries, the patient succumbed to cardiogenic shock 5 days later.

Recommended Resources

Disclaimer

Cases come from all over the world. Patient identifiers have been redacted or patient consent has been obtained. The contents of this site have not been reviewed nor approved by Hennepin County Medical Center and any views or opinions expressed herein do not necessarily reflect the views or opinions of Hennepin County Medical Center.